Objective To investigate effect and mechanism of probiotic products on α-naphthylisothiocyanate(ANIT) induced intrahepatic cholestasis of weaned rats through the changes of gastrointestine myoelectric migrating complexes(MMC).Methods Ninety-six SD rats were randomly divided into 3 groups:control group(n=16),intoxication group(n=40)and intervention group(n=40).Three pairs of bipolar silver electrodes were chronically implanted in the antrum,duodenum and jejunum of 8 rats from every group.Sham operation was given to the others of the 3 groups.Seven to 10 days after operation,all rats of intoxication and intervention groups received a single intragastric administration of ANIT(200 mg/kg)in order to induce acute intrahepatic cholestasis.Probiotic products,4.2×108/(kg·d),was given to intervention group 2 days before ANIT was administrated.The gastrointestinal MMC was recorded in conscious and fasting state every 48 h till 192 h after ANIT was given.Biliary flow,total bilirubin(TB) and ALT was recorded in sham operated rats at the same time.Results 1.Forty-eight hours after ANIT was gavaged,the biliary flow of intoxication and intervention groups decreased while ALT and TB increased.But the above observed indexes of intoxication group were more significantly altered than those of intervention group.2.A typical MMC pattern could be seen in all normal conscious fasting rats and it disappeared temporarily after ANIT was given.Ninety-six to 192 h later,the MMC pattern recovered gradually and intervention group′s MMC pattern appeared earlier than that of the intoxication group.But increased MMC cycle duration was seen in the intoxication group at 192 h and it was characterized by an increased duration of phase Ⅱ-like activity.Conclusions MMC pattern disappeared or the duration of MMC become longer when acute cholestasis was induced with ANIT in rats.Probiotic products can promote the initiation of MMC and decrease the cycle duration,thereby relieve the cholestasis.

Objective To study the expression of soluble intercellular adhesion molecule-1(sICAM-1) in rabbits′ model of acute intrahepatic cholestasis and its significance.Methods Thirty-nine newborn rabbits were divided randomly into 4 groups:3 experimental groups(n=9) and a control group(n=12).A single dose(200 mg/kg) of α-naphthylisothiocyanate(ANIT) was administered by ga-(vage) to each experimental rabbit to induce intrahepatic cholestasis.The specimens of serum and bile were collected from rabbits at 24,48,and 72 h after intoxication and sICAM-1 was detected by enzyme linked immunosorbent assay(ELISA).Results Compared with control group,the sICAM-1 in serum and bile of experimental groups were significantly increased 48 h72 h24 h(all P0.05).Conclusions Acute intrahepatic cholestasis induced by ANIT results in alterations of sICAM-1 in serum and bile.The alternation may be used to estimate the injury of hepatobiliary system.

小儿感染性休克起病急、进展迅速,病死率高.早期诊断及识别一些危险因素,及时给予有力的干预措施,是降低病死率的关键.

AIM: To investigate the changes of gastrointestinal interdigestive migrating myoelectric complex (MMC) in the weaned rat models of acute intrahepatic cholestasis induced by alphanaphthyl-isothiocyanate (ANIT). METHODS: A total of 56 weaned Sprague Dawley rats were randomly divided into two groups: control group (n = 16) and toxication group (n = 40). Three pairs of bipolar silver electrodes were chronically implanted in the antrum, duodenum and jejunum of 8 rats from each group in random. Sham operation was performed in the other rats of both groups. Seven to ten days after the operation, MMC was recorded in all the rats with implanted electrodes. Then, all of the rats in toxication group received a single intragastric administration of ANIT (200 mg/kg) in order to induce acute intrahepatic cholestasis. The gastrointestinal MMC was recorded in conscious and fasting status 48, 96, 144, 192 h after ANIT was given. The levels of biliary flow, total bilirubin (TB) and alanine aminotransferase (ALT) were recorded at the same time. RESULTS: Forty-eight hours after ANIT was given, the biliary flow of rats in toxication group was almost ceased completely while the levels of ALT and TB were increased remarkably. Then, they were all improved gradually till the 192 hour. A typical MMC pattern was seen in all the normal conscious and fasting rats, and disappeared temporarily after ANIT was given. One hundred and forty-four hours later, the MMC pattern began to restore gradually and recovered at the 192 hour. However, the prolonged cycle duration of MMC (911.67 ± 140.47 s vs 682.87 ± 77.39 s, P < 0.05) was observed in the toxication group at the 192 hour and characterized by an increased duration of phase II-like activity (414.12 ± 69.21 s vs 150.28 ± 35.45 s, P < 0.05) and decreased duration of phase III activity (121.21 ± 27.38 s vs 170.27 ± 38.98 s, P < 0.05). CONCLUSION: MMC disappearance followed by a prolonged MMC is the pattern of MMC changes in the weaned rats with ANIT-induced intrahepatic cholestasis, and this may be related with the decrease of bile flow during the interdigestive periods.

Objective To study the alternation of SIgA in serum and bile in experimental acute intrahepatic cholestasis. Method 39 newborn rabbits were divided at random into four groups: 3 experimental groups (n=9) and a contral group (n=12). A single dose (200 mg/kg) of ANIT(α-naphthyl isothiocyanate) was administered by gavage to each experimental rabbit to induce intrahepatic cholestasis. The specimens of serum and bile were collected from rabbits at 24 h, 48 h and 72 h after intoxication and detected by SIgA radioimmunologic kit. Result Compared with the control group.the SIgA in serum of experimental groups began to increase 24 h after intoxication(P< 0.05 ),then were getting singnificantly higher(P< 0.01 ).And the concentration of bile SIgA decreased dramatically(P< 0.01 ) . Conclusion Acute intrahepatic cholestasis induced by ANIT resulted in alterations of SIgA in serum and bile, and the alternation may be used to estimate the injury of hepatobiliary system.

在哺乳动物体内有两型肿瘤坏死因子-α(TNF-α)共同存在,一种是以细胞膜结合分子的形式表达于细胞表面的跨膜型TNF-α(tmTNF-α),另一种是广泛分布的可溶性TNF-α(sTNF-α).tmTNF-α作为sTNF-α的前体,在适当的条件下被金属蛋白酶切割而释放至体液中形成sTNF-α.研究发现tmTNF-α虽然是sTNF-α的前体,但与其释放后形成的可溶性形式在很多方面有差异.现就其特殊的生物学活性和其在一些疾病中所起的作用综述如下.